The persistence of SARS-CoV-2-attributable mortality into the post-PHEIC period is not paradoxical, even in the context of widespread vaccination, frequent reinfection, and substantially improved clinical management. Improvements in the acute management of COVID-19 act most directly on deaths coded as COVID-19; our regression-based approach, however, is deliberately agnostic to cause-of-death coding. A growing body of evidence indicates that SARS-CoV-2 infection precipitates downstream cardiovascular, cerebrovascular, and thrombotic events, as well as secondary and reactivated infections, that may prove fatal but are recorded under causes other than COVID-19 and are largely unaffected by improvements in acute COVID-19 care. Deaths arising through these pathways are systematically under-captured by cause-of-death-specific approaches but are detectable in models relating all-cause mortality to viral circulation; our own analyses link SARS-CoV-2 activity to downstream events including pulmonary embolism and invasive group A streptococcal disease. This mechanism parallels the influenza-attributable burden recorded under non-respiratory causes discussed above. Persistence of attributable mortality is further consistent with waning population protection: vaccine uptake in Canada fell substantially beyond the primary series, and protection against SARS-CoV-2 is transient, reflecting both antigenic change and immune waning, with severity of outcomes predicted by recency of vaccination as well as cumulative dose number. A population with low uptake of additional vaccine doses and increasingly remote from its most recent dose would retain limited vaccine-derived protection, providing no expectation that attributable mortality would decline through the post-PHEIC period.